By the time individuals enter a clinical setting for treatment of a dysfunctional habit - whether directed toward food, gambling, drugs of abuse, or sex - the behavior has not only been acquired, but overlearned. In order to treat such behaviors, it is not sufficient to understand the neurobiological circuits controlling acquisition nd expression of behavior during early stages of learning. The long-term objective of this work is to understand the changes that occur within brain circuits mediating reward-directed behavior as it becomes over-learned. Preliminary data show that dopamine D1 receptor transmission within the nucleus accumbens core mediates cued approach to a reward location during early stages of learning, but not after the behavior has been well acquired. In this proposal we test the hypotheses that neural substrates mediating the reward-directed behavior A) remain in the accumbens while the role of dopamine transmission in the region diminishes (the accumbens early and late model), or B) no longer involves the accumbens (substrate shift model). Three specific aims attack these two hypotheses by 1) examining the cued approach response following blockade of dopamine receptors within the accumbens core or shell during either early or extended stages of training, 2) examining the effect of accumbens core or shell deactivation during early vs late stages of training, and 3) examining how individual neurons in the accumbens core and shell respond during the behavior after extended training. Unique sets of results will distinguish the two models above, as well as a third (hybrid) model in which the accumbens continues to mediate the learned behavior while additional parallel circuits come to mediate the response as well.